Politis-Barber 2020 Am J Physiol Endocrinol Metab

From Bioblast
Publications in the MiPMap
Politis-Barber V, Brunetta HS, Paglialunga S, Petrick HL, Holloway GP (2020) Long-term high-fat feeding exacerbates short-term increases in adipose mitochondrial reactive oxygen species, without impairing mitochondrial respiration. Am J Physiol Endocrinol Metab 319:E376-87.

Β» PMID: 32543945 Open Access

Politis-Barber Valerie, Brunetta Henver S, Paglialunga Sabina, Petrick Heather L, Holloway Graham P (2020) Am J Physiol Endocrinol Metab

Abstract: White adipose tissue (WAT) dysfunction in obesity is implicated in the onset of whole-body insulin resistance. Alterations in mitochondrial bioenergetics, namely impaired mitochondrial respiration and increased mitochondrial reactive oxygen species (mtROS) production, have been suggested to contribute to this metabolic dysregulation. However, techniques investigating mitochondrial function are classically normalized to tissue weight, which may be confounding when considering obesity-related adipocyte hypertrophy. Furthermore, the effect of long-term high-fat diet (HFD) on mtROS in WAT has yet to be elucidated. Therefore, we sought to determine the HFD-mediated temporal changes in mitochondrial respiration and mtROS emission in WAT. C57BL/6N mice received low-fat diet or HFD for 1 or 8 weeks and changes in inguinal WAT (iWAT) and epididymal WAT (eWAT) were assessed. While tissue weight-normalized mitochondrial respiration was reduced in iWAT following 8 weeks HFD-feeding, this effect was mitigated when adipocyte cell-size and/or number were considered. These data suggest HFD does not impair mitochondrial respiratory capacity per adipocyte within WAT. In support of this assertion, within eWAT compensatory increases in lipid-supported and maximal succinate-supported respiration occurred at 8-weeks despite cell hypertrophy and increases in WAT inflammation. Although these data suggest impairments in mitochondrial respiration do not contribute to HFD-mediated WAT phenotype, lipid-supported mtROS emission increased following 1-week HFD in eWAT, while both lipid and carbohydrate-supported mtROS were increased at 8 weeks in both depots. Combined, these data establish that while HFD does not impair adipocyte mitochondrial respiratory capacity, increased mtROS is an enduring physiological occurrence within WAT in HFD-induced obesity. β€’ Keywords: High-fat diet, Insulin resistance, Mitochondrial function, Obesity, White adipose tissue β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: CA Guelph Holloway GP

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Obesity 

Organism: Mouse  Tissue;cell: Fat  Preparation: Permeabilized cells 

Coupling state: LEAK, OXPHOS  Pathway: F, N, Gp, NS  HRR: Oxygraph-2k 


Cookies help us deliver our services. By using our services, you agree to our use of cookies.